Cognitive models in a fuller understanding of schizophrenia.
There is a gap in scientific understanding of psychiatric disorders such as schizophrenia, between neurophysiological models of etiology and the behavioral expressions of the disorders. More complete cognitive models are needed to fill that gap. Such models would set neurophysiological models in a more meaningful context, would show how biological processes produce social-behavioral impairments, and would inform both biological and psychosocial treatment strategies. To be fully functional, however, cognitive models must address two key principles: diathesis-stress in the course of schizophrenia, and the nature of reciprocal causality in complex, self-regulating biosystems.
Spaulding
W D
WD
Department of Psychology, University of Nebraska-Lincoln 68588-0308, USA.
D003072:Cognition Disorders / Q000209:etiology* / Q000523:psychology; D019336:Cognitive Science; D004198:Disease Susceptibility; D006801:Humans; D008960:Models, Psychological; D012559:Schizophrenia / Q000150:complications / Q000209:etiology* / Q000503:physiopathology; D012565:Schizophrenic Psychology; D012920:Social Behavior Disorders / Q000209:etiology* / Q000523:psychology